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目的:探讨线粒体融合蛋白2(Mfn2)在环孢素A(CSA)引起的慢性肾损伤中的作用及可能的机制。方法:制作慢性CSA肾病大鼠模型，将大鼠分为溶剂对照组、CSA模型组和正常对照组。分别检测各组大鼠血肌酐及尿蛋白水平。光镜检查观察肾小管间质损伤情况。电镜观察肾小管上皮内线粒体结构改变，Western blot检测肾组织Mfn2蛋白的表达。结果:CSA模型组造模2、4周血肌酐和尿蛋白水平较正常对照组和溶剂对照组均明显升高(n P<0.05)。CSA模型组肾小管间质损伤明显，肾小管上皮细胞内可见线粒体肿胀变形，脊消失。CSA模型组2、4周肾组织Mfn2蛋白的表达明显降低，与正常对照组和溶剂对照组相比差异有统计学意义(n P<0.05)；与2周模型组比较，4周组Mfn2蛋白的表达进一步减少(n P<0.05)。n 结论:Mfn2可能在CSA引起的肾小管上皮细胞损伤中发挥重要作用。“,”Objective:This study aimed to investigate the role of mitochondrial fusion protein 2 (Mfn2) in chronic renal injury caused by cyclosporine A (CSA) and the possible mechanism.Methods:The model of chronic CSA nephropathy was established in rats. The rats were divided into solvent control group, CSA model group and normal control group. Serum creatinine and urinary protein levels were detected. The tubulointerstitial injury was observed by light microscopy. The changes of mitochondrial structure were observed by electron microscope, and the expression of Mfn2 was detected by Western blot.Results:The levels of serum creatinine and urinary protein in CSA model group at 2 and 4 weeks were significantly higher than those in control group and solvent group (n P<0.05). In CSA model group, tubulointerstitial injury was obvious, mitochondria swelling and deformation were found in tubular epithelial cells, and ridge disappeared. Compared with normal control group and solvent control group, the expression of Mfn2 in CSA model group was significantly decreased at 2 and 4 weeks (n P<0.05), and the expression of Mfn2 in CSA model group at 4 weeks was further decreased compared with 2 weeks (n P<0.05).n Conclusions:Mfn2 may play an important role in the injury of tubular epithelial cells caused by cyclosporine.